COVID-19 and Kidney Injury

R I Med J (2013). 2020 Sep 4;103(8):24-28.

Abstract

Acute kidney injury (AKI) has been reported as a complication of COVID-19. However, the epidemiology, management, and associated outcomes have varied greatly between studies. The pathophysiology remains unclear. Summary: The etiology of AKI in the setting of COVID-19 appears multifactorial. Systemic effects of sepsis, inflammation, and vascular injury likely play some role. Furthermore, SARS-CoV-2 binds to the angiotensin-converting enzyme 2 receptor, highly expressed in the kidney, providing a route for direct infection. Older age, baseline comorbidities, and respiratory failure are strong risk factors for the development of AKI. Regardless of etiology, AKI carries a significantly increased risk for in-hospital mortality, especially in those with critical illness. Currently, management of AKI in patients with COVID-19 remains supportive. Key Messages: AKI is common in patients with COVID-19. Future studies are needed to examine the response to anti-viral treatment as well as long-term renal outcomes in patients with AKI.

Keywords: ACE2; COVID-19; acute kidney injury.

MeSH terms

  • Acute Kidney Injury* / etiology
  • Acute Kidney Injury* / mortality
  • Acute Kidney Injury* / therapy
  • Acute Kidney Injury* / virology
  • Angiotensin-Converting Enzyme 2
  • Betacoronavirus* / isolation & purification
  • Betacoronavirus* / physiology
  • COVID-19
  • Coronavirus Infections* / epidemiology
  • Coronavirus Infections* / physiopathology
  • Coronavirus Infections* / therapy
  • Coronavirus Infections* / virology
  • Critical Illness* / mortality
  • Critical Illness* / therapy
  • Hospital Mortality
  • Humans
  • Kidney* / metabolism
  • Kidney* / virology
  • Pandemics*
  • Patient Care Management / methods*
  • Peptidyl-Dipeptidase A / metabolism
  • Pneumonia, Viral* / epidemiology
  • Pneumonia, Viral* / physiopathology
  • Pneumonia, Viral* / therapy
  • Pneumonia, Viral* / virology
  • Prognosis
  • Risk Assessment
  • Risk Factors
  • SARS-CoV-2
  • Virus Internalization

Substances

  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2